Appendix A
sodium excretion refl ects the fact that much sodium
reabsorption by the proximal tubule is achieved by
countertransport. By blocking hydrogen ion
secretion, therefore, the drug also partially blocks
sodium reabsorption. The increased water excretion
occurs because the failure to reabsorb sodium and
bicarbonate decreases water reabsorption (remember
that water reabsorption is secondary to solute
reabsorption), resulting in an osmotic diuresis.
Chapter 15
Test Questions
15-1 c
When the stomach contents, which are very acidic,
move into the small intestine, it stimulates the
release of secretin, which circulates to the pancreas
and stimulates the release of bicarbonate into the
small intestine. This neutralizes the acid and protects
the small intestine.
15-2 d
GIP release is a feedforward mechanism to signal the
islet cells in the pancreas that the products of food
digestion are on their way to the blood. This results
in an augmented insulin response to a meal.
15-3 a
Gastrin is a major controller of acid secretion by the
stomach. When the stomach becomes very acidic,
gastrin release is inhibited, preventing continued acid
15-4 b
Cholecystokinin is the primary signal from the
small intestine to the pancreas to increase digestive
enzyme release into the small intestine.
15-5 d
The enzyme pepsin is produced from pepsinogen
in the presence of acid. This zymogen accelerates
protein digestion.
15-6 b
Because fat is insoluble in an aqueous environment,
micelles keep fat droplets from re-aggregating and
small enough to be absorbed.
15-7 c
Distention of the duodenum signals the stomach
that the meal has moved on and continued acid
secretion in the stomach is not necessary until the
next meal.
15-8 a
Bicarbonate in the bile is secreted by the epithelial
cells lining the bile ducts.
15-9 e
Although the primary movement of chyme in
segmentation is back and forth, the overall, net
movement of chyme is from the small intestine to
the large intestine.
15-10 a
The active transport of sodium in the large intestine
is the driving force for the osmotic absorption of
Quantitative and Thought Questions
If the salivary glands fail to secrete amylase, the
undigested starch that reaches the small intestine
will still be digested by the amylase the pancreas
secretes. Thus, starch digestion is not signifi cantly
affected by the absence of salivary amylase.
Alcohol can be absorbed across the stomach wall,
but absorption is much more rapid from the small
intestine with its larger surface area. Ingestion of
foods containing fat releases enterogastrones from the
small intestine, and these hormones inhibit gastric
emptying and thus prolong the time alcohol spends in
the stomach before reaching the small intestine. Milk,
contrary to popular belief, does not “protect” the
lining of the stomach from alcohol by coating it with
a fatty layer. Rather, the fat content of milk decreases
the rate of absorption of alcohol by decreasing the rate
of gastric emptying.
Vomiting results in the loss of fl
uid and acid
from the body. The fl uid comes from the luminal
contents of the stomach and duodenum, most of
which was secreted by the gastric glands, pancreas,
and liver and thus is derived from the blood.
The cardiovascular symptoms of this patient are
the result of the decrease in blood volume that
accompanies vomiting.
The secretion of acid by the stomach produces
an equal number of bicarbonate ions, which are
released into the blood. Normally these bicarbonate
ions are neutralized by hydrogen ions released into
the blood by the pancreas when this organ secretes
bicarbonate ions. Because gastric acid is lost during
vomiting, the pancreas is not stimulated to secrete
bicarbonate by the usual high-acidity signal from
the duodenum, and no corresponding hydrogen
ions are formed to neutralize the bicarbonate
released into the blood by the stomach. As a
result, the acidity of the blood decreases. Loss of
potassium from the loss of stomach contents can
also lead to hypokalemia.
Fat can be digested and absorbed in the absence of
bile salts, but in greatly decreased amounts. Without
adequate emulsifi cation of fat by bile salts and
phospholipids, only the fat at the surface of large lipid
droplets is available to pancreatic lipase, and the rate
of fat digestion is very slow. Without the formation of
micelles with the aid of bile salts, the products of fat
digestion become dissolved in the large lipid droplets,
where they are not readily available for diffusion into the
epithelial cells. In the absence of bile salts, only about
50 percent of the ingested fat is digested and absorbed.
The undigested fat is passed on to the large intestine,
where bacteria produce compounds that increase colonic
motility and promote the secretion of fl uid into the
lumen of the large intestine, leading to diarrhea.
Damage to the lower portion of the spinal cord
produces a loss of voluntary control over defecation
due to disruption of the somatic nerves to the
skeletal muscle of the external anal sphincter.
Damage to the somatic nerves leaves the external
sphincter in a continuously relaxed state. Under
these conditions, defecation occurs whenever the
rectum becomes distended and the defection refl ex is
Vagotomy decreases the secretion of acid by the
stomach. Impulses in the parasympathetic nerves
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